Role of the Herpes Simplex Virus 1 Internal Repeat Sequences in Pathogenicity

Jenkins, Frank J.; Martin, John R.

doi:10.1159/000150147

Cited by 12 publications

(7 citation statements)

References 4 publications

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“…These mutant forms of the genomes of HSV-1 and CMV and now EHV-1 that fail to undergo isomerization are capable of replication in cell culture with an efficiency similar to that of wild type virus. However, the v11LΔIR mutant exhibited a significant reduction in pathogenicity in the mouse, and these findings are similar to the situation with the noninverting HSV-1 mutant that was found to be profoundly attenuated in vivo (Jenkins et al,1996; Jenkins and Martin, 1990). Since the vL11ΔIR has reduced virulence in vivo , it would be of interest to ascertain if this mutant virus has the ability to spread to the central nervous system and/or establish latency in the natural host.…”

Section: Discussionsupporting

confidence: 64%

Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region

et al. 2011

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The 150 kbp genome of equine herpesvirus -1 (EHV-1) is composed of a unique long (UL) region and a unique short (Us) segment, which is flanked by identical internal and terminal repeat (IR and TR) sequences of 12.7kbp. We constructed an EHV-1 lacking the entire IR (vL11ΔIR) and showed that the IR is dispensable for EHV-1 replication but that the vL11ΔIR exhibits a smaller plaque size and delayed growth kinetics. Western blot analyses of cells infected with vL11ΔIR showed that the synthesis of viral proteins encoded by the immediate-early, early, and late genes was reduced at immediate-early and early times, but by late stages of replication reached wild type levels. Intranasal infection of CBA mice revealed that the vL11ΔIR was significantly attenuated as mice infected with the vL11ΔIR showed a reduced lung viral titer and greater ability to survive infection compared to mice infected with parental or revertant virus.

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Section: Discussionsupporting

confidence: 64%

Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region

et al. 2011

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“…That is to say that peripheral replication of HSV may induce a non-permissive environment for viral replication in neurons innervating the site of replication. Animal models using corneal infections, have demonstrated that infectious HSV is not detected within trigeminal ganglia until 48 ± 72 h post-infection (Coen et al, 1989;Jenkins and Martin, 1990;Tenser and Edris, 1987). This delay would allow for the establishment of a IL-1/NGF/Oct-2-mediated non-permissive environment.…”

Section: A Viral Vector For Gene Therapymentioning

confidence: 99%

The roles of herpes simplex virus in neuroscience

Turner¹,

Jenkins²

1997

J Neurovirol

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Herpes simplex virus (HSV) has been a focus of research in many laboratories during the last 30 ± 35 years, with the majority centered on the virus' replication, molecular biology and pathogenesis. Recently, HSV has begun to receive considerable attention in the field of neuroscience, where scientists have begun to use the virus as a tool or model for several areas of investigation. These areas include the construction and development of HSV-based vectors for gene therapy and the use of HSV as a neuronal tracer, as a model for demyelinating disease and to study interactions between the nervous, immune and endocrine systems. The goal of this paper is to review these different roles for HSV in the broad field of neuroscience.

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“…Recombinant mutants of HSV-1 that are not able to undergo homologous recombination due to the deletion of part or all of the inverted repeats at the junction between the L and S fragments (a=b=/a=c=) showed lower efficiency of replication in vitro than the corresponding wild-type virus and an absence of acute infection in vivo (27,28,41,46). These observations suggest that either the doubled rate of synthesis of proteins encoded by the b=a=/a=c= sequences and/or the ability to undergo homologous recombination is required for efficient in vivo infection.…”

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confidence: 99%

Structural Variability of the Herpes Simplex Virus 1 Genome In Vitro and In Vivo

Mahiet

Ergani

Huot

et al. 2012

J Virol

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dHerpes simplex virus 1 (HSV-1) is a human pathogen that leads to recurrent facial-oral lesions. Its 152-kb genome is organized in two covalently linked segments, each composed of a unique sequence flanked by inverted repeats. Replication of the HSV-1 genome produces concatemeric molecules in which homologous recombination events occur between the inverted repeats. This mechanism leads to four genome isomers (termed P, IS, IL, and ILS) that differ in the relative orientations of their unique fragments. Molecular combing analysis was performed on DNA extracted from viral particles and BSR, Vero, COS-7, and Neuro-2a cells infected with either strain SC16 or KOS of HSV-1, as well as from tissues of experimentally infected mice. Using fluorescence hybridization, isomers were repeatedly detected and distinguished and were accompanied by a large proportion of noncanonical forms (40%). In both cell and viral-particle extracts, the distributions of the four isomers were statistically equivalent, except for strain KOS grown in Vero and Neuro-2a cells, in which P and IS isomers were significantly overrepresented. In infected cell extracts, concatemeric molecules as long as 10 genome equivalents were detected, among which, strikingly, the isomer distributions were equivalent, suggesting that any such imbalance may occur during encapsidation. In vivo, for strain KOS-infected trigeminal ganglia, an unbalanced distribution distinct from the one in vitro was observed, along with a considerable proportion of noncanonical assortment.

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Role of the Herpes Simplex Virus 1 Internal Repeat Sequences in Pathogenicity

Cited by 12 publications

References 4 publications

Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region

Properties of an equine herpesvirus 1 mutant devoid of the internal inverted repeat sequence of the genomic short region

The roles of herpes simplex virus in neuroscience

Structural Variability of the Herpes Simplex Virus 1 Genome In Vitro and In Vivo

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